scholarly journals Innate immune molecule surfactant protein D attenuates sepsis‐induced acute kidney injury through modulating apoptosis and NFκB‐mediated inflammation

2019 ◽  
Vol 17 (1) ◽  
pp. 100-106 ◽  
Author(s):  
Shi‐Jun Lu ◽  
Jian‐Hua Xu ◽  
Zhao‐Feng He ◽  
Peng Wu ◽  
Chao Ning ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Surfactant Protein ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Immune Molecule

scholarly journals Expression of Surfactant Protein D in the Human Gastric Mucosa and during Helicobacter pylori Infection

2002 ◽  
Vol 70 (3) ◽  
pp. 1481-1487 ◽  
Author(s):  
Emma Murray ◽  
Wafa Khamri ◽  
Marjorie M. Walker ◽  
Paul Eggleton ◽  
Anthony P. Moran ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Surfactant Protein ◽  
Normal Mucosa ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Human Gastric Mucosa ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Immune Molecule ◽  
H Pylori

ABSTRACT Helicobacter pylori establishes persistent infection of gastric mucosa with diverse clinical outcomes. The innate immune molecule surfactant protein D (SP-D) binds selectively to microorganisms, inducing aggregation and phagocytosis. In this study, we demonstrated the expression of SP-D in gastric mucosa by reverse transcription-PCR and immuohistochemical analysis. SP-D is present at the luminal surface and within the gastric pits, with maximal expression at the surface. Levels of expression are significantly increased in H. pylori-associated gastritis compared to those in the normal mucosa. Immunofluorescence microscopy was used to demonstrate binding and agglutination of H. pylori by SP-D in a lectin-specific manner. These activities resulted in a 50% reduction in the motility of H. pylori, as judged on the basis of curvilinear velocity measured by using a Hobson BacTracker. Lipopolysaccharides extracted from three H. pylori strains were shown to bind SP-D in a concentration-dependent manner, and there was marked variation in the avidity of binding among the strains. SP-D may therefore play a significant role in the innate immune response to H. pylori infection.

scholarly journals Toll-like Receptor 7 Contributes to Inflammation, Organ Injury, and Mortality in Murine Sepsis

2019 ◽  
Vol 131 (1) ◽  
pp. 105-118 ◽  
Author(s):  
Wenling Jian ◽  
Lili Gu ◽  
Brittney Williams ◽  
Yan Feng ◽  
Wei Chao ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Immune Responses ◽  
Knockout Mice ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Innate Immune ◽  
Organ Injury ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Wild Type

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Sepsis remains a critical illness with high mortality. The authors have recently reported that mouse plasma RNA concentrations are markedly increased during sepsis and closely associated with its severity. Toll-like receptor 7, originally identified as the sensor for single-stranded RNA virus, also mediates host extracellular RNA-induced innate immune responses in vitro and in vivo. Here, the authors hypothesize that innate immune signaling via Toll-like receptor 7 contributes to inflammatory response, organ injury, and mortality during polymicrobial sepsis. Methods Sepsis was created by (1) cecal ligation and puncture or (2) stool slurry peritoneal injection. Wild-type and Toll-like receptor 7 knockout mice, both in C57BL/6J background, were used. The following endpoints were measured: mortality, acute kidney injury biomarkers, plasma and peritoneal cytokines, blood bacterial loading, peritoneal leukocyte counts, and neutrophil phagocytic function. Results The 11-day overall mortality was 81% in wild-type mice and 48% in Toll-like receptor 7 knockout mice after cecal ligation and puncture (N = 27 per group, P = 0.0031). Compared with wild-type septic mice, Toll-like receptor 7 knockout septic mice also had lower sepsis severity, attenuated plasma cytokine storm (wild-type vs. Toll-like receptor 7 knockout, interleukin-6: 43.2 [24.5, 162.7] vs. 4.4 [3.1, 12.0] ng/ml, P = 0.003) and peritoneal inflammation, alleviated acute kidney injury (wild-type vs. Toll-like receptor 7 knockout, neutrophil gelatinase-associated lipocalin: 307 ± 184 vs.139 ± 41-fold, P = 0.0364; kidney injury molecule-1: 40 [16, 49] vs.13 [4, 223]-fold, P = 0.0704), lower bacterial loading, and enhanced leukocyte peritoneal recruitment and phagocytic activities at 24 h. Moreover, stool slurry from wild-type and Toll-like receptor 7 knockout mice resulted in similar level of sepsis severity, peritoneal cytokines, and leukocyte recruitment in wild-type animals after peritoneal injection. Conclusions Toll-like receptor 7 plays an important role in the pathogenesis of polymicrobial sepsis by mediating host innate immune responses and contributes to acute kidney injury and mortality.

scholarly journals Sex and SP-A2 Dependent NAD(H) Redox Alterations in Mouse Alveolar Macrophages in Response to Ozone Exposure: Potential Implications for COVID-19

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 915
Author(s):  
He N. Xu ◽  
Zhenwu Lin ◽  
Chintan K. Gandhi ◽  
Shaili Amatya ◽  
Yunhua Wang ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Imaging Technique ◽  
Redox Balance ◽  
Surfactant Protein ◽  
Redox Status ◽  
Innate Immune ◽  
Ozone Exposure ◽  
Dependent Manner ◽  
Immune Molecule ◽  
Air Control

Co-enzyme nicotinamide adenine dinucleotide (NAD(H)) redox plays a key role in macrophage function. Surfactant protein (SP-) A modulates the functions of alveolar macrophages (AM) and ozone (O3) exposure in the presence or absence of SP-A and reduces mouse survival in a sex-dependent manner. It is unclear whether and how NAD(H) redox status plays a role in the innate immune response in a sex-dependent manner. We investigated the NAD(H) redox status of AM from SP-A2 and SP-A knockout (KO) mice in response to O3 or filtered air (control) exposure using optical redox imaging technique. We found: (i) In SP-A2 mice, the redox alteration of AM in response to O3 showed sex-dependence with AM from males being significantly more oxidized and having a higher level of mitochondrial reactive oxygen species than females; (ii) AM from KO mice were more oxidized after O3 exposure and showed no sex differences; (iii) AM from female KO mice were more oxidized than female SP-A2 mice; and (iv) Two distinct subpopulations characterized by size and redox status were observed in a mouse AM sample. In conclusions, the NAD(H) redox balance in AM responds to O3 in a sex-dependent manner and the innate immune molecule, SP-A2, contributes to this observed sex-specific redox response.

2P-0395 Surfactant protein D of the innate immune defense is negatively associated with obesity

2003 ◽  
Vol 4 (2) ◽  
pp. 125
Author(s):  
U. Holmskov ◽  
G. Lyster ◽  
J. Hjelmborg ◽  
R. Leth-Larsen ◽  
V. Moeller ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Immune Defense ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Negatively Associated ◽  
Innate Immune Defense

Circulating Surfactant Protein D Is Decreased in Systemic Lupus Erythematosus

2009 ◽  
Vol 36 (11) ◽  
pp. 2449-2453 ◽  
Author(s):  
SILJE VERMEDAL HOEGH ◽  
ANNE VOSS ◽  
GRITH LYKKE SORENSEN ◽  
ANETTE HØJ ◽  
CHRISTIAN BENDIXEN ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Surfactant Protein ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Systemic Lupus ◽  
Reactive Protein ◽  
Structural And Functional Properties ◽  
Disease Indicators ◽  
And Function

Objective.Deficiencies of innate immune molecules like mannan binding lectin (MBL) have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). Surfactant protein D (SP-D) and MBL belong to the same family of innate immune molecules — the collectins, which share important structural and functional properties. We aimed to compare concentrations of serum SP-D in patients with SLE and in healthy controls, and to investigate if SP-D is associated with selected disease indicators. We investigated the possible association of the Met11Thr polymorphism with disease, since this polymorphism is an important determinant for serum level, oligomerization pattern, and function of SP-D.Methods.Serum SP-D was measured using a 5-layer ELISA in 70 SLE patients and 1476 healthy subjects. DNA was genotyped for the Met11Thr variant.Results.Median SP-D level in serum was 911 ng/ml (95% CI 776–1118) in patients and 1068 ng/ml (95% CI 901–1246) in controls (p = 0.0004). Circulating SP-D did not differ significantly in patients with high, intermediate, or low SLE disease activity. Similarly, SP-D did not correlate with C-reactive protein, erythrocyte sedimentation rate, and anti-dsDNA seropositivity. Genetic analysis did not support an association of the Met11Thr genotype with SLE.Conclusion.These findings suggest that low SP-D, unrelated to conventional disease indicators, represents an aspect of SLE etiopathogenesis.

scholarly journals Innate Immune Collectin Surfactant Protein D Enhances the Clearance of DNA by Macrophages and Minimizes Anti-DNA Antibody Generation

2005 ◽  
Vol 174 (11) ◽  
pp. 7352-7358 ◽  
Author(s):  
Nades Palaniyar ◽  
Howard Clark ◽  
Jeya Nadesalingam ◽  
Michael J. Shih ◽  
Samuel Hawgood ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Innate Immune ◽  
Surfactant Protein D
Sign in / Sign up

Export Citation Format

Share Document